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Chronic thromboembolic disease (CTED) is suboptimally defined by a mean pulmonary artery pressure (mPAP) <25 mmHg at rest in patients that remain symptomatic from chronic pulmonary artery thrombi. To improve identification of right ventricular (RV) pathology in patients with thromboembolic obstruction, we hypothesized that the RV ventriculo‐arterial (Ees/Ea) coupling ratio at maximal stroke work (Ees/Eamax sw) derived from an animal model of pulmonary obstruction may be used to identify occult RV dysfunction (low Ees/Ea) or residual RV energetic reserve (high Ees/Ea). Eighteen open chested pigs had conductance catheter RV pressure‐volume (PV)‐loops recorded during PA snare to determine Ees/Eamax sw. This was then applied to 10 patients with chronic thromboembolic pulmonary hypertension (CTEPH) and ten patients with CTED, also assessed by RV conductance catheter and cardiopulmonary exercise testing. All patients were then restratified by Ees/Ea. The animal model determined an Ees/Eamax sw = 0.68 ± 0.23 threshold, either side of which cardiac output and RV stroke work fell. Two patients with CTED were identified with an Ees/Ea well below 0.68 suggesting occult RV dysfunction whilst three patients with CTEPH demonstrated Ees/Ea ≥ 0.68 suggesting residual RV energetic reserve. Ees/Ea > 0.68 and Ees/Ea < 0.68 subgroups demonstrated constant RV stroke work but lower stroke volume (87.7 ± 22.1 vs. 60.1 ± 16.3 mL respectively, P = 0.006) and higher end‐systolic pressure (36.7 ± 11.6 vs. 68.1 ± 16.7 mmHg respectively, P < 0.001). Lower Ees/Ea in CTED also correlated with reduced exercise ventilatory efficiency. Low Ees/Ea aligns with features of RV maladaptation in CTED both at rest and on exercise. Characterization of Ees/Ea in CTED may allow for better identification of occult RV dysfunction. We have used PV‐loop analysis in a porcine model of pulmonary hypertension to define the optimal Ees/Ea coupling ratio for RV maximal efficiency. We have applied this cut‐off to patients with chronic thromboembolic pulmonary disease and detected occult RV dysfunction.

Meerkats (Suricata suricatta) are routinely anesthetized with isoflurane in zoo and field settings. Twenty healthy adult meerkats of mixed age and sex held in the Zoological Society of London's collection were anesthetized with 4% isoflurane by face mask for routine health examinations. The procedure was repeated 5 mo later in the same group of animals utilizing sevoflurane at 5% for induction, and again 3 mo later with sevoflurane at 6.5% for induction to approximate equipotency with isoflurane. The speed and quality of induction and recovery were compared between the two volatile anesthetic agents. There was no statistically significant difference in the speed of induction across any of the anesthetic regimes. There was a significant difference in recovery times between isoflurane and 6.5% sevoflurane (427 ± 218 and 253 ± 65 sec, respectively [mean ± SD]). Under the conditions of this study, sevoflurane at 6.5% induction dose resulted in better quality induction and recovery than sevoflurane at 5% induction or isoflurane. The mean heart and respiratory rates during anesthesia were higher using 5% sevoflurane for induction but there was no significant difference in either rate between isoflurane and sevoflurane used at a 6.5% induction dose. This study suggests that sevoflurane at a dose of 6.5% for induction and 4% for maintenance is a safe and effective anesthetic agent in healthy adult meerkats. Rapid return to normal behavior after anesthesia is important in all zoo species but particularly so in animals with a complex social and hierarchical structure such as meerkats. For this species, the advantage afforded by the speed of recovery with sevoflurane may offset the cost in certain circumstances.

This study aims to describe the anaesthetic management of dogs undergoing mitral valve repair under cardiopulmonary bypass (CPB) and to evaluate the peri-anaesthetic morbidity and mortality of this procedure. This manuscript presents a retrospective, observational, descriptive cohort analysis performed at a tertiary university hospital. Medical records of dogs that had undergone mitral valve repair under CPB between August 2017 and June 2024 were examined. Demographic data, perioperative data and complications were recorded. All statistical analyses were conducted in R. The primary endpoint was all-cause mortality before discharge (dead vs. alive at discharge). Descriptive statistic and univariable and multivariable logistic regression models using Firth's penalised maximum likelihood were fitted. A total of 176 dogs underwent CPB for surgical correction of myxomatous mitral valve disease. Perioperative complications were frequent. Certain complications, particularly refractory arrhythmias and low cardiac output events, were often fatal despite aggressive intervention. The overall mortality before discharge was 20.5% (4.0% intraoperatively and 16.5% postoperatively before discharge). Lower body weight, longer CPB time and severe tricuspid regurgitation were factors associated with higher mortality. Surgical repair of the mitral valve in dogs can be associated with serious intraoperative and postoperative complications. Careful case selection is warranted, particularly in dogs with severe tricuspid regurgitation, low body weight, or other markers of advanced disease. Where feasible, CPB duration should be minimised, and vigilant perioperative monitoring with rapid-response protocols for anticipated complications should be implemented.

Acute liver failure is a rare but catastrophic condition which can progress rapidly to multi-organ failure. Studies investigating the onset of individual organ injury such as the liver, kidneys and brain during the evolution of acute liver failure, are lacking. MicroRNAs are short, non-coding strands of RNA that are released into the circulation following tissue injury. In this study, we have characterised the release of both global microRNA and specific microRNA species into the plasma using a porcine model of acetaminophen-induced acute liver failure. Pigs were induced to acute liver failure with oral acetaminophen over 19h±2h and death occurred 13h±3h thereafter. Global microRNA concentrations increased 4h prior to acute liver failure in plasma (P<0.0001) but not in isolated exosomes, and were associated with increasing plasma levels of the damage-associated molecular pattern molecule, genomic DNA (P<0.0001). MiR122 increased around the time of onset of acute liver failure (P<0.0001) and was associated with increasing international normalised ratio (P<0.0001). MiR192 increased 8h after acute liver failure (P<0.0001) and was associated with increasing creatinine (P<0.0001). The increase in miR124-1 occurred concurrent with the pre-terminal increase in intracranial pressure (P<0.0001) and was associated with decreasing cerebral perfusion pressure (P<0.002). Conclusions: MicroRNAs were released passively into the circulation in response to acetaminophen-induced cellular damage. A significant increase in global microRNA was detectable prior to significant increases in miR122, miR192 and miR124-1, which were associated with clinical evidence of liver, kidney and brain injury respectively.

Increases in prothrombin time (PT) and international normalised ratio (INR) characterise acute liver injury (ALI) and failure (ALF), yet a wide heterogeneity in clotting abnormalities exists. This study defines evolution of coagulopathy in 10 pigs with acetaminophen (APAP)-induced ALI compared to 3 Controls. APAP administration began at 0 h and continued to ‘ALF’, defined as INR >3. In APAP pigs, INR was 1.05 ± 0.02 at 0 h, 2.15 ± 0.43 at 16 h and > 3 at 18 ± 1 h. At 12 h thromboelastography (TEG) demonstrated increased clot formation rate, associated with portal vein platelet aggregates and reductions in protein C, protein S, antithrombin and A Disintegrin and Metalloprotease with Thrombospondin type 1 repeats–13 (ADAMTS-13) to 60%, 24%, 47% and 32% normal respectively. At 18 ± 1 h, INR > 3 was associated with: hypocoagulable TEG profile with heparin-like effect; falls in thrombin generation, Factor V and Factor VIII to 52%, 19% and 17% normal respectively; further decline in anticoagulants; thrombocytopenia; neutrophilia and endotoxemia. Multivariate analysis, found that ADAMTS-13 was an independent predictor of a hypercoagulable TEG profile and platelet count, endotoxin, Protein C and fibrinogen were independent predictors of a hypocoagulable TEG profile. INR remained normal in Controls. Dynamic changes in coagulation occur with progression of ALI: a pro-thrombotic state progresses to hypocoagulability.

Acute liver failure is a rare but catastrophic condition which can progress rapidly to multi-organ failure. Studies investigating the onset of individual organ injury such as the liver, kidneys and brain during the evolution of acute liver failure, are lacking. MicroRNAs are short, non-coding strands of RNA that are released into the circulation following tissue injury. In this study, we have characterised the release of both global microRNA and specific microRNA species into the plasma using a porcine model of acetaminophen-induced acute liver failure. Pigs were induced to acute liver failure with oral acetaminophen over 19h plus or minus 2h and death occurred 13h plus or minus 3h thereafter. Global microRNA concentrations increased 4h prior to acute liver failure in plasma (P<0.0001) but not in isolated exosomes, and were associated with increasing plasma levels of the damage-associated molecular pattern molecule, genomic DNA (P<0.0001). MiR122 increased around the time of onset of acute liver failure (P<0.0001) and was associated with increasing international normalised ratio (P<0.0001). MiR192 increased 8h after acute liver failure (P<0.0001) and was associated with increasing creatinine (P<0.0001). The increase in miR124-1 occurred concurrent with the pre-terminal increase in intracranial pressure (P<0.0001) and was associated with decreasing cerebral perfusion pressure (P<0.002). Conclusions MicroRNAs were released passively into the circulation in response to acetaminophen-induced cellular damage. A significant increase in global microRNA was detectable prior to significant increases in miR122, miR192 and miR124-1, which were associated with clinical evidence of liver, kidney and brain injury respectively.